aristolochic acid/rak

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New molecular and field evidences for the implication of mycotoxins but not aristolochic acid in human nephropathy and urinary tract tumor.

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To find out whether ochratoxin A (OTA), citrinin (CIT), aristolochic acids (AA) are etiologic agents of Balkan endemic nephropathy (BEN) or Chinese herbal nephrotoxicity, and associated urinary tract tumor (UTT), we have compared (i) in human kidney cell culture, the DNA adduct formation and

Gene expression profiles modulated by the human carcinogen aristolochic acid I in human cancer cells and their dependence on TP53.

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Aristolochic acid (AA) is the causative agent of urothelial tumours associated with aristolochic acid nephropathy. These tumours contain TP53 mutations and over-express TP53. We compared transcriptional and translational responses of two isogenic HCT116 cell lines, one expressing TP53 (p53-WT) and

[Influence of taking aristolochic acid-containing Chinese drugs on occurrence of urinary transitional cell cancer in uremic uremic patients undergoing dialysis].

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OBJECTIVE To investigate the prevalence and clinical characteristics of urinary transitional cell cancer (TCC) in uremic patients undergoing dialysis who have history of taking aristolochic acid (AA)-containing Chinese drugs. METHODS A questionnaire survey was conducted among 283 uremic patients

Increased risk of urinary tract cancer in ESRD patients associated with usage of Chinese herbal products suspected of containing aristolochic acid.

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BACKGROUND Both end-stage renal disease (ESRD) and urothelial cancer (UC) are associated with the consumption of Chinese herbal products containing aristolochic acid (AA) by the general population. The objective of this study was to determine the risk of UC associated with AA-related Chinese herbal

Transitional cell carcinoma associated with aristolochic acid nephropathy: most common cancer in chronic hemodialysis patients in China.

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BACKGROUND The research of cancer in patients on hemodialysis (HD) in China has not been reported. The aim of this study was to investigate the clinical and histological features and outcomes of cancer in Chinese HD patients. METHODS The study subjects were 49 cancer patients (1.4%) out of 3448 end

Y27632 attenuates the aristolochic acid-promoted invasion and migration of human urothelial cancer TSGH cells in vitro and inhibits the growth of xenografts in vivo.

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BACKGROUND Aristolochic acid I (AAI) has been implicated in urothelial cell carcinoma (UCC) in humans. However, whether AAI promotes invasion/migration of UCC has not been established. METHODS A study of human UCC TSGH cells cultured with AAI was conducted. Cell viability, the effects of AAI on the

TP53 mutation signature supports involvement of aristolochic acid in the aetiology of endemic nephropathy-associated tumours.

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The proposal has been put forward that the primary cause of Balkan endemic nephropathy (BEN) is exposure to food crops contaminated with seeds of Aristolochia spp, which contain high levels of aristolochic acids (AA). Recently, tumour DNA samples from patients with BEN were found to harbour

Analysis of potential risk factors for cancer incidence in patients with aristolochic acid nephropathy from Wenzhou, China.

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BACKGROUND The purpose of this study was to investigate the cancer incidence in patients with end-stage aristolochic acid nephropathy (AAN). METHODS A total of 102 patients with end-stage AAN treated in our hospital between 2004 and 2013 were included in this study. The correlation of cancer

Evidence of exposure to aristolochic acid in patients with urothelial cancer from a Balkan endemic nephropathy region of Romania.

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Recently, chronic Aristolochia poisoning was found responsible for the aetiology of Balkan endemic nephropathy (BEN) in Croatia, Serbia, and Bosnia, and diet was the likely route of exposure to aristolochic acid (AA). BEN, often associated with an increased incidence of upper urinary tract carcinoma

The Mutational Features of Aristolochic Acid-Induced Mouse and Human Liver Cancers.

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Aristolochic acid (AA) exposure has been statistically associated with human liver cancers. However, direct evidence of AA exposure-induced liver cancer is absent. This study aims to establish a direct causal relationship between AA exposure and liver cancers based on a mouse model and

Aristolochic acid-associated urothelial cancer in Taiwan.

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Aristolochic acid, a potent human carcinogen produced by Aristolochia plants, is associated with urothelial carcinoma of the upper urinary tract (UUC). Following metabolic activation, aristolochic acid reacts with DNA to form aristolactam (AL)-DNA adducts. These lesions concentrate in the renal

Mutation signatures implicate aristolochic acid in bladder cancer development.

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BACKGROUND Aristolochic acid (AA) is a natural compound found in many plants of the Aristolochia genus, and these plants are widely used in traditional medicines for numerous conditions and for weight loss. Previous work has connected AA-mutagenesis to upper-tract urothelial cell carcinomas and

Aristolochic acid as a probable human cancer hazard in herbal remedies: a review.

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The old herbal drug aristolochic acid (AA), derived from Aristolochia spp., has been associated with the development of a novel nephropathy, designated aristolochic acid nephropathy (AAN), and urothelial cancer in AAN patients. There is clear evidence that the major components of the plant extract

Aristolochic acids and their derivatives are widely implicated in liver cancers in Taiwan and throughout Asia.

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Many traditional pharmacopeias include Aristolochia and related plants, which contain nephrotoxins and mutagens in the form of aristolochic acids and similar compounds (collectively, AA). AA is implicated in multiple cancer types, sometimes with very high mutational burdens, especially in upper

Revealing a Pre-neoplastic Renal Tubular Lesion by p-S6 Protein Immunohistochemistry after Rat Exposure to Aristolochic Acid.

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Aristolochic acid (AA) has, in the last decade, become widely promoted as the cause of the Balkan endemic nephropathy and associated renal or urothelial tumours, although without substantial focal evidence of the quantitative dietary exposure via bread in specific households in hyperendemic

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